Submitted on January 16, 2008
Accepted on April 10, 2008
DIFFERENCES IN INTRAGASTRIC pH IN DIABETIC VERSUS IDIOPATHIC GASTROPARESIS: RELATION TO DEGREE OF GASTRIC RETENTION
William L. Hasler1*, Radoslav Coleski1, William D. Chey2, Kenneth L. Koch3, Richard W. McCallum4, John M Wo5, Braden Kuo6, Michael D Sitrin7, Leonard A Katz8, Judy Hwang9, John R Semler9, and Henry P Parkman10
1 Gastroenterology, University of Michigan Health System, Ann Arbor, Michigan, United States
2 Gastroenterology, University of Michigan, Ann Arbor, Michigan, United States
3 Section on Gastroenterology, Wake Forest University School of Medicine, Winston-Salem, North Carolina, United States
4 Gastroenterology, University of Kansas Medical Center, United States
5 Gastroenterology, University of Louisville Medical Center, Louisville, Kentucky, United States
6 Gastroenterology, Massachusetts General Hospital, Boston, Massachusetts, United States
7 Gastroenterology, Western New York VA Medical Center, Buffalo, New York, United States
8 Gastroenterology, University of Buffalo School of Medicine, Buffalo, New York, United States
9 SmartPill Corporation, Buffalo, New York, United States
10 Gastroenterology, Temple University School of Medicine, Philadelphia, Pennsylvania, United States
* To whom correspondence should be addressed. E-mail: whasler{at}umich.edu.
Evidence suggests that distinct mechanisms underlie diabetic and idiopathic gastroparesis. Differences in gastric acid in gastroparesis of different etiologies and varying degrees of gastric stasis are uninvestigated. We tested the hypotheses that (i) gastric pH profiles show differential alteration in diabetic vs. idiopathic gastroparesis and (ii) abnormal pH profiles relate to the severity of gastric stasis. Sixty-four healthy controls and 44 gastroparesis patients (20 diabetic, 24 idiopathic) swallowed wireless transmitting capsules then consumed 99mTc-sulfur colloid-labeled meals for gastric scintigraphy. Gastric pH from the capsule was recorded every 5 seconds. Basal pH was higher in diabetics (3.64±0.41) versus controls (1.90±0.18) and idiopathics (2.41±0.42)(P<0.05). Meals evoked initial pH increases that were greater in diabetics (4.98±0.32) than idiopathics (3.89±0.39)(P=0.03) but not controls (4.48±0.14). pH nadirs prior to gastric capsule evacuation were higher in diabetics (1.50±0.23) than controls (0.58±0.11)(P=0.003). Four hour gastric retention was similar in diabetic (18.3±0.5%) and idiopathic (19.4±0.5%) patients but higher than controls (2.2±0.5%)(P<0.001). Compared to controls, those with moderate-severe stasis (>20% retention at 4 hours) had higher basal (3.91±0.55) and nadir pH (2.23±0.42) values (P<0.05). In subgroup analyses, both diabetics and idiopathics with moderate-severe gastroparesis exhibited increased pH parameters versus those with mild gastroparesis. In conclusion, diabetics with gastroparesis exhibit reduced gastric acid, an effect more pronounced in those with severely delayed gastric emptying. Idiopathic gastroparetics exhibit nearly normal acid profiles, although those with severely delayed emptying show reduced acid versus those with mild delays. Thus, both etiology and degree of gastric stasis determine gastric acidity in gastroparesis.
